Member Biography

We are interested in understanding the molecular mechanisms by which inherited mutations in the transcription factor GATA2 lead to GATA2 deficiency syndrome and Acute Myeloid Leukemia (AML). To this end, we have developed a novel Gata2T354M knock-in mouse model and are using multi-omic approaches. This aim is part of a broader strategy to identify and functionally pathways regulated by GATA2 that are functionally relevant for the pathogenesis of Acute Myeloid Leukemia, and to develop novel ways to manipulate these pathways for therapeutic benefit.